Intranuclear localization of the transcription coadaptor CBP/p300 and the transcription factor RBP-Jk in relation to EBNA-2 and -5 in B lymphocytes

We have studied the expression and the localization of the cellular proteins CBP/p300 and RBP-Jk in in vitro EBV-infected human B lymphocytes in relation to the EBNA-2 and EBNA-5 proteins. We found that the level of CBP/p300 was elevated drastically by EBV infection and also after activation by CD40 ligation. Thus the increase in CBP/p300 expression in the EBV-infected cells is related to the virus-induced activation and proliferation of the cells. EBNA-2 and RBP-Jk colocalized in the nucleoplasm, which is in accordance with their functional interaction. We confirmed earlier reports about the presence and colocalization of EBNA-5 and CBP in the nuclear POD bodies. On the other hand, neither EBNA-2 nor p300 was detected in the PODs. The expression of these two proteins overlapped in some distinct dots of the nucleoplasm. Taken together, the different patterns of CBP and p300 expression and their different localization in relation to the PML bodies and two EBV-encoded proteins in the B cells may provide some clue to their distinct functional roles.     

Clinicopathological significance of SIRT1 and p300/CBP expression in gastroesophageal junction (GEJ) cancer and the correlation with E-cadherin and MLH1

SIRT1 and p300/CBP, which are considered to be essential histone deacetylases and acetyltransferases, are also considered to be relative to tumorigenesis because they modulate the expression of several tumor suppressor genes. Therefore, this study investigated the expression of SIRT1 and p300/CBP in gastroesophageal junction (GEJ) cancer and their correlation with E-cadherin and MLH1 in order to explore the clinicopathological significance of SIRT1 and p300/CBP expression and their possible effects involving E-cadherin and MLH1 expression. Tissue microarray technique and immunohistochemical stains were applied to evaluate the SIRT1, p300/CBP, E-cadherin, and MLH1 expression in 176 GEJ cancer tissues and 32 normal GEJ region tissues. The results showed that the over-expression of SIRT1 was associated with a higher number of metastasis lymph nodes, more advanced staging, and shorter mean survival time. SIRT1 and p300/CBP were negatively and positively correlated with the expression of E-cadherin and MLH1, respectively, in the cancer cases. These results indicated a possible effect of SIRT1 and p300/CBP involved in regulating the expression of E-cadherin and MLH1, thus participating in the tumor progression of GEJ cancer.